Coordinated muscle activity patterns in the lower limb determine, in part, the reaction force of the limb against the support surface. Our lab has shown that there is inappropriate coordination of muscle activity in post-stroke locomotion and that the reaction force against the supporting surface is compromised, in both magnitude and direction. These compromised forces destabilize the body during locomotion and place individuals with post-stroke hemiplegia at high risk for frequent falls and femoral fractures. Thus, it is necessary to study muscle coordination patterns to identify the underlying causative mechanisms that impair locomotor capability post-stroke. It has been proposed by several investigators that a putative mechanism contributing to the emergence of altered muscle coordination in post-stroke limb movement is the withdrawal of brainstem inhibition due to the stroke-induced loss of cortico-spinal and cortico-bulbar fibers. Moreover, the investigation of the activity of spinal neural circuits after stroke during a unilateral pedaling task showed that pedaling with only one limb generated rhythmic alternating muscle activity in the opposite resting limb and the phenomenon is more pronounced in the most impaired individuals. This is postulated to be further evidence for an increase reliance on bulbospinal pathways, which are know to project bilaterally in the spinal cord. In an effort to test this conceptual framework we intend to implement the following specific aims: Specific Aim 1: To test the hypothesis that the unintended muscle activity in the resting paretic limb of post- stroke individuals (while the opposite nonparetic limb pedals) is an expression of an increased reliance on brainstem pathways which involves increased abnormal muscle coupling as compared to controls and is stronger at high levels of force effort. Specific Aim 2: To test the hypothesis that the unintended muscle coactivation patterns during a unilateral pedaling task of the opposite limb underlies the discoordination of bilateral pedaling post-stroke. We will use principal component analysis on electromyograms of 16 lower limb muscles bilaterally to identify groups of active muscles in post-stroke hemiparetic individuals and controls. We will test the hypotheses using non-parametic statistics and statistics on the frequency distribution of active muscles under the conditions tested. Successful completion of these aims will support the similarity between unintended activity in the control of locomotion and previously reported changes in upper limb control post-stroke. Results of our proposed study will constitute a mechanistic rationale for the use of body weight supported treadmill training (BWSTT) and constraint induced movement therapy (CIMT). [unreadable] [unreadable] [unreadable]